nee joints [J]. Rheumatol, 2003, 30(3):559566.
[2]彭丹,孙材江. 实验性骨关节病中软骨细胞的凋亡 [J]. 湖南医科大学学报, 1999, 24(5):415417.
[3]Stefanovic RM, Stadler J, Evans CH, et al. Nitric oxide and arthritis [J]. Arthr Rheum, 1993, 36(8):10361044.
[4]Jang D, Murrell GA. Nitric oxide in arthritis [J]. Free Radic Biol Med, 1998, 24(9):15111519.
[5]Lotz M. The role of nitric oxide in articular cartilage damage [J]. Rheum Dis Clin North Am, 1999, 25(2):269282.
[6]Hashimoto S, Setareh M, Ochs RL, et al. Fas/Fas ligand expression and induction of apoptosis in chondrocytes [J]. Arthr Rheum, 1997, 40(10):17491755.
[7]Presle N, Cipolletta C, Jouzeau JY, et al. Cartilage protection by nitric oxide synthase inhibitors after intraarticular injection of interleukin1 beta in rats [J]. Arthr Rheum, 1999, 42(10):20942102.
[8]Pelletier J, Jovanovic D, Fermandes JC, et al. Reduction in the structural changes of experimental osteoarthritis by a nitric oxide inhibitor [J]. Osteoarthr Cartilage, 1999, 7(4):416418.
[9]McCartneyFrancis NL, Song X, Mizel DE, et al.Selective inhibition of inducible nitric oxide synthase exacerbates erosive joint disease [J]. Immumol, 2001, 166(4):27342740.
[10]Tilton RG, Chang K, Hasan KS, et al. Prevention of diabetic vascular dysfunction by guanidines. Inhibition of nitric oxide synthase versus advanced glycation endproduct formation [J]. Diabetes, 1993, 42(2):221232.
[11]Wolff DJ, Lubeskie A. Aminoguanidine is an isoformselective, mechanismbased inactivator of nitric oxide synthase [J]. Arch Biochem Biophys, 1995, 316(1):290301.
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